Annals of Epidemiology xxx (2015) 1e5

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Annals of Epidemiology
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Brief communication

Birth weight, fetal growth, and risk of pediatric rhabdomyosarcoma:

an updated record linkage study in California
Libby M. Morimoto PhD a, *, Kathryn McCauley MPH a, Xiaomei Ma PhD b, Joseph L. Wiemels PhD c,
Anand P. Chokkalingam PhD a, Catherine Metayer MD PhD a
a
Division of Epidemiology, School of Public Health, University of California, Berkeley
b
Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT
c
Department of Epidemiology and Biostatistics, University of California, San Francisco

a r t i c l e i n f o a b s t r a c t

Article history: Purpose: The purpose of the study was to examine whether birth characteristics affect the risk of
Received 15 July 2015 rhabdomyosarcoma (RMS) in children and adolescents younger than 19 years.
Accepted 27 November 2015 Methods: A total of 722 RMS cases diagnosed at the age of 0e19 years during 1988e2011 were identified
from the California Cancer Registry and matched by birth date, sex, and race to 2,888 controls using
California birth records. Conditional logistic regression was used to estimate the risk of RMS associated
Keywords:
with birth weight, gestational age, and size for gestational age.
Pediatric rhabdomyosarcoma
Results: High birth weight (odds ratio [OR]: 1.00; 95% confidence interval [CI]: 0.78e1.29) and large for
Birth weight
Fetal growth
gestational age (LGA; OR: 0.94, 95% CI: 0.72e1.23) were not associated with RMS risk overall. Among
non-Hispanic whites, the ORs were 1.33 for high birth weight (95% CI: 0.94e1.89) and 1.17 for LGA (95%
CI: 0.78e1.75); no indications of association were observed for other racial or ethnic groups (P interaction
<.10). Compared with normal gestational age, preterm (<37 weeks) and post-term (>40 weeks) babies
had 16%e18% lower risks of RMS overall, after adjusting for birth weight.
Conclusions: In the largest study to date, there was an indication of association between high birth
weight, LGA, and increased RMS risk among non-Hispanic white children and adolescents, but not in
other racial or ethnic groups.
Ó 2015 Elsevier Inc. All rights reserved.

Introduction and is more common in males than females (1.5:1), whereas

Rhabdomyosarcoma (RMS) is the most common soft tissue
sarcoma affecting children and adolescents (age, 0e19 years), with
approximately five cases per million diagnosed annually in the
United States [1]. Pediatric RMS arises from skeletal muscle tissue;
two major subtypes, embryonal (eRMS) and alveolar RMS (aRMS),
make up 60%e75% and 16%e30% of total cases, respectively [2e4].
Owing to the rarity of pediatric RMS, little is known about its
etiology. Most RMS cases are sporadic, with a small proportion
associated with genetic syndromes, including Li-Fraumeni,
neurofibromatosis, and Beckwith-Wiedemann syndromes [5].
The incidence for embryonal subtype peaks before 5 years of age,
* Corresponding author. Division of Epidemiology, UC Berkeley School of Public
Health, 1995 University Avenue, Suite 460, Berkeley, CA 94704. Tel.: þ1-510-642-
6299; fax: þ1-510-643-1735.
E-mail address: libbym@berkeley.edu (L.M. Morimoto).
alveolar incidence is evenly distributed throughout childhood and
adolescence [5, 6]. Recent studies suggest an association with
accelerated fetal growth. In a study of 27 cases, proportions of
optimal birth weight and optimal weight for length were asso-
ciated with increased risk, although associations were not sta-
tistically significant [7]. A record linkage study of 583 children
(age, 0e5 years) diagnosed with RMS in California, Minnesota,
New York, Texas, and Washington from 1988 to 1997 reported
associations with high birth weight (odds ratio [OR]: 1.27, 95%
confidence interval [CI]: 1.14e1.42) and the top decile of size for
gestational age (OR: 1.42, 95% CI: 1.03e1.96) [8]. A statewide
California study of 359 RMS cases aged 0e4 years, diagnosed from
1988 and up to 2008, showed a nonstatistically significant
association between high birth weight and eRMS (OR: 1.21; 95%
CI: 0.81e1.81), but not aRMS (OR: 0.60; 95% CI: 0.24e1.50) [9]. In
contrast, an analysis of 322 matched cases and controls from the
Intergroup Rhabdomyosarcoma Study Group (age, 0e20 years)

http://dx.doi.org/10.1016/j.annepidem.2015.11.007
1047-2797/Ó 2015 Elsevier Inc. All rights reserved.

Please cite this article in press as: Morimoto LM, et al., Birth weight, fetal growth, and risk of pediatric rhabdomyosarcoma: an updated record
linkage study in California, Annals of Epidemiology (2015), http://dx.doi.org/10.1016/j.annepidem.2015.11.007
2 L.M. Morimoto et al. / Annals of Epidemiology xxx (2015) 1e5

Table 1
Risk of rhabdomyosarcoma associated with birth characteristics among 722 cases and 2888 controls in California (1988e2011)

Characteristic All RMS (n cases ¼ 722, n controls ¼ 2,888) eRMS (n cases ¼ 444, n aRMS (n cases ¼ 197, n P for
controls ¼ 1,776) controls ¼ 788) interactiony

Controls, Cases, OR* (95% CI) Controls, Cases, OR* (95% CI) Controls, Cases, OR* (95% CI)
n (%) n (%) n (%) n (%) n (%) n (%)
Birth weight (g)
Low (<2,500) 164 (6) 48 (7) 1.05 (0.73e1.50) 95 27 0.99 (0.63e1.55) 53 13 0.97 (0.51e1.84) .09
Normal (2,500 2,362 (82) 585 (81) 1.00 (Ref.) 1,466 356 1.00 (Ref.) 635 164 1.00 (Ref.)
e4,000)
High (>4,000) 362 (13) 89 (12) 1.00 (0.78e1.29) 215 61 1.09 (0.81e1.47) 100 20 0.89 (0.55e1.44)
P-trend .88 .61 .72
Gestational age (wk)
Preterm (<37) 278 (10) 67 (9) 0.84 (0.62e1.12) 175 40 0.82 (0.57e1.19) 76 16 0.66 (0.38e1.16) .30
Normal (37e40) 1,300 (45) 355 (49) 1.00 (Ref.) 796 217 1.00 (Ref.) 363 103 1.00 (Ref.)
Overdue (>40) 1,134 (39) 252 (35) 0.82 (0.68e0.98) 701 158 0.84 (0.67e1.05) 300 64 0.70 (0.50e0.97)
Missing 176 (6) 48 (7) 1.01 (0.72e1.41)
P-trend .27 .51 .35
Size for gestational age
Small for gestational 277 (10) 73 (10) 1.00 (0.76e1.32) 177 41 0.91 (0.64e1.30) 78 24 1.25 (0.78e1.98) .22
age
Appropriate for 2,099 (73) 523 (72) 1.00 (Ref.) 1,294 325 1.00 (Ref.) 573 139 1.00 (Ref.)
gestational age
Large for gestational 336 (12) 78 (11) 0.94 (0.72e1.23) 201 49 0.96 (0.69e1.33) 88 20 0.94 (0.58e1.53)
age
Missing 176 (6) 48 (7) 1.10 (0.79e1.53) 0.38
P-trend .60 .84

* Odds ratios are adjusted for plurality.

y
P for interaction from likelihood-ratio test comparing eRMS versus aRMS.

enrolled from 1982 to 1988 observed statistically significant as-
sociations between both low (OR: 4.46; 95% CI: 1.41e14.1) and
high (OR: 2.41; 95% CI: 1.09e5.35) birth weight and aRMS,
although no statistically significant associations were seen for the
more common embryonal subtype [5].
The present analysis is an update to previous analyses of RMS
cases conducted in California; it includes diagnoses spanning
24 years (1988e2011) and ages to 19 years, more than doubling the
sample size of earlier studies [8, 10]. This is the largest study
examining the association between birth weight, measures of fetal
growth, and risk of RMS overall and by race and ethnic group and
histologic subtype.
Methods
Study population
We conducted a population-based case-control study of 722
cases of pediatric RMS (International Classification of Childhood
Cancer, third edition, recode 91; International Classification of Dis-
eases for Oncology, third edition (ICD-O-3), codes 8900e8905, 8910,
8912, 8920, 8991) and 2,888 matched controls by linking cancer
diagnosis records from the California Cancer Registry (CCR) to birth
records maintained by the vital statistics unit of the California
Department of Public Health. Cases were diagnosed from 1988 (the
earliest year the CCR data were electronically available) through
2011 (when the linkage was conducted) and born in or after 1978
(the earliest year the California birth data were electronically
available), and each case was linked to statewide birth records and
matched by year and month of birth, sex, race, and ethnicity (i.e.,
Hispanic vs. non-Hispanic) to four controls from the birth records
who had not been linked to the CCR. Using first and last name, date
of birth, mother’s name, and social security number (when avail-
able), 76% of RMS cases were linked to a California birth certificate.
This study was approved by Institutional Review Boards at the
University of California, Berkeley and the California Department of
Public Health.
Data collection
The California birth records included data on sociodemographic,
birth, and pregnancy characteristics, including birth weight (in
grams) and gestation length (in days), birth order, plurality, race
and ethnicity (child, maternal, and paternal), parental age and years
of education, geographic location at birth, month when prenatal
care began, and principal source of payment for prenatal care and
delivery. The CCR data included information on the date of cancer
diagnosis and tumor characteristics.
Gestational age was calculated from the date of last menstrual
period through birth date. Outlier values less than 20 weeks or
greater than 43 weeks were removed (n ¼ 73). Size for gestational
age was calculated according to the methodology described in
Alexander et al. [11]. Briefly, information from the pool of all
available “healthy” controls was used to establish standards strat-
ified by week of gestation, sex, and race. Any child above the 90th or
below the 10th percentile for birth weight in their gestational week,
sex, and race-specific strata was considered to be large for gesta-
tional age (LGA) or small for gestational age (SGA).
Cancer histologic type was classified as embryonal (ICD-O-3:
8910, 8912, 8991), alveolar (8920), or unclassified (8900e8902).
Cancer site was classified according to the ICD-O-3 Surveillance
Epidemiology and End Results (SEER) Site/Histology Validation List
codes (http://seer.cancer.gov/icd-o-3/sitetype.icdo3.d20150918.
pdf), as connective and soft tissue (ICD-10: C470eC476,
C478eC479, C490eC496, C498eC499), testis (C620eC6221, C629),
orbit (eye; C690eC691, C693, C695eC698), nasopharynx
(C110eC113, C118eC119), and others.
Statistical analysis
Statistical analyses used both univariate and multivariate con-
ditional logistic regression to calculate ORs and 95% CIs for each
measure of fetal growth, including birth weight (<2,500,
2,500e4,000, >4,000 g), gestational age (premature, <37 weeks;
normal, 3740 weeks; overdue, >40 weeks), and size for
 L.M. Morimoto et al. / Annals of Epidemiology xxx (2015) 1e5 3

gestational age (SGA, appropriate for gestational age, LGA) for total

interactionx
RMS, and for eRMS and aRMS subtypes separately. Demographic
and birth characteristics, including maternal age and race, birth
P for

.057

.170

.025
order, plurality, and start of prenatal care, were assessed as poten-
tial confounders; only plurality changed risk estimates more than
1.96 (0.62e6.25)

0.89 (0.29e2.73)

1.46 (0.55e3.90)

0.91 (0.48e1.73)

1.57 (0.71e3.51)

0.72 (0.28e1.88)
10%. The final model included only plurality, conditioning on birth
OR* (95% CI)

1.00 (Ref.) year, child’s sex, and child’s race. Analyses were stratified by child’s

1.00 (Ref.)

1.00 (Ref.)
race, age at diagnosis or reference age, birth decade, season of birth,
and cancer site. Local regression smoothed curves were constructed
Asian (n cases ¼ 71, n

.34

.46

.18
to portray the proportion of cases at different birth weight, gesta-
controls ¼ 285)

tional age, and birth weight adjusted for gestational age, separately
Cases/controls

for Hispanics and non-Hispanic whites, representing the nonpara-

metric trend of RMS risk associated with these measures.
59/253

37/160

48/202
7/13

5/19

8/21

20/85

11/28

6/36
Results
interactionz

The 722 RMS cases and 2,888 age, sex, and race and ethnicity-
matched controls were similar in most demographic and birth
P for

.061

.247

.052

characteristics, although mothers and fathers of cases tended to be

slightly older and more educated at the child’s birth (data not
1.16 (0.54e2.50)

0.49 (0.16e1.47)

0.98 (0.46e2.11)

0.94 (0.49e1.78)

1.01 (0.40e2.50)

0.60 (0.25e1.39)

shown). Sixty-one percent of cases were classified as embryonal,

OR* (95% CI)

27% alveolar, and 11% unclassified. Half of the cancers were located
1.00 (Ref.)

1.00 (Ref.)

1.00 (Ref.)

in connective and soft tissue, 7% in the testis, 7% in the orbit, and 6%

Black, (n cases ¼ 71, n

in the nasopharynx. Approximately 29 additional sites were iden-

.24

.88

.34

tified (31% of cases) but were not considered because of small

controls ¼ 286)

Cases/controls

numbers.
Neither high birth weight (>4,000 g; OR: 1.00; 95% CI: 0.78e1.29)
56/220

31/126

50/190

nor LGA (>90%; OR: 0.94, 95% CI: 0.72e1.23) was associated with
11/35

4/31

11/41

23/93

8/27

7/43

increased risk of total RMS, relative to normal birth weight

(2,500e4,000 g) and appropriate for gestational age (10th%e90th%),
interactiony

respectively (Table 1). The risk of RMS among children whose

gestational age was more than 40 weeks was 18% lower than normal
P for

.147

.254

.077
Risk of childhood rhabdomyosarcoma associated with birth characteristics, stratified by child’s race (1988e2011)

gestational age (37e40 weeks) (OR: 0.82, 95% CI: 0.68e0.98), even
after adjusting for birth weight. This trend, however, was not linear,
1.01 (0.57e1.80)

0.78 (0.50e1.22)

0.94 (0.60e1.47)

0.76 (0.56e1.01)

1.33 (0.87e2.02)

0.87 (0.55e1.38)

with preterm babies (born <37 weeks) having a nonstatistically

P for interaction from likelihood-ratio test comparing white versus Hispanic and black populations.
OR* (95% CI)

significant inverse association (OR: 0.84, 95% CI: 0.62e1.12). In

1.00 (Ref.)

1.00 (Ref.)

1.00 (Ref.)
Hispanic (n cases ¼ 288, n

subtype-specific analysis, there was a suggestion of differential ef-

fect estimates for birth weight and eRMS (OR: 1.09, 95% CI:
.35

.12

.16

P for interaction from likelihood-ratio test comparing white versus Hispanic populations.

0.63e1.55) and aRMS (OR: 0.89, 95% CI: 0.55e1.44), although the
controls ¼ 1,149)

interaction was not statistically significant (P ¼ .09).

Odds ratios are adjusted for plurality; matching factors are birth date, sex, and race.
Cases/controls

Table 2 shows analyses stratified by child’s race. There was a

245/958
26/131

31/116
146/520
91/446

34/104

25/119
209/859

suggestion that high birth weight (OR: 1.33, 95% CI: 0.94e1.89, P-
17/60

P for interaction from likelihood-ratio test comparing white versus all races.

trend: .08) and LGA (OR: 1.17, 95% CI: 0.78e1.75, P-trend: .10) were
positively associated with total RMS risk among non-Hispanic
whites, but not other racial or ethnic groups (P-interaction ¼ .06
0.83 (0.42e1.64)

1.33 (0.94e1.89)

0.57 (0.32e1.02)

0.86 (0.65e1.15)

0.69 (0.41e1.15)

1.17 (0.78e1.75)

for birth weight; P-interaction ¼ .03 for SGA). The lack of an asso-
OR* (95% CI)

1.00 (Ref.)

1.00 (Ref.)

1.00 (Ref.)

ciation was most notable among Hispanics, the largest racial or

White (n cases ¼ 281, n

ethnic group in the analysis, where high birth weight (OR: 0.78, 95%
.08

.74

.10

CI: 0.50e1.22, P-trend: .35) and LGA (OR: 0.87, 95% CI: 0.55e1.38, P-
controls ¼ 1,121)

trend: .16) were unrelated to risk. The effect was even more pro-
Cases/controls

nounced when limited to eRMS, although cell sizes for histology

and race-stratified results were small (data not shown). The rela-
214/895
54/172

132/470
117/492

20/112
206/813
39/133
All RMS

13/54

16/96

tionship between longer or shorter gestational age (relative to

normal duration) and RMS did not differ by race and ethnicity, with
all groups having a nonstatistically significant inverse association.
Appropriate for gestational age

We further explored this apparent effect modification by race and

ethnicity by constructing smoothed spline curves separately for
Small for gestational age

Large for gestational age

Normal (2,500e4,000)

Hispanics and non-Hispanic whites (Fig. 1). For birth weight and
Size for gestational age

birth weight adjusted for gestational age, risk of RMS increased

Gestational age (wk)

Normal (37e40)

with increasing birth weight (up to w5000 g) among non-Hispanic

Overdue (>40)
Preterm (<37)
High (>4,000)
Birth weight (g)
Low (<2,500)

whites, whereas among Hispanics, the trend was flat or in the

Characteristic

opposite direction. There was no evidence that the relationship of

P-trend

P-trend

P-trend

any of the fetal growth measures and RMS differed by age at

Table 2

diagnosis (<6 years vs. 6 years), cancer site (connective tissue vs.
y
z
x
*

testis), or decade or season of birth (data not shown).

4 L.M. Morimoto et al. / Annals of Epidemiology xxx (2015) 1e5
Fig. 1. Proportion of rhabdomyosarcoma cases across (A) birth weight, (B) gestational age, and (C) birth weight/gestational age.
Discussion
In the largest study of pediatric RMS to date, we found an
indication of association between high birth weight, LGA, and
increased RMS risk, particularly eRMS, among non-Hispanic white
children and adolescents, but not in other racial or ethnic groups.
This result supports the associations observed in previous studies,
with analyses of primarily white populations yielding stronger
positive associations with birth weight [5, 8] compared to studies
with large Hispanic representations [10]. In addition, we observed
some evidence that longer or shorter periods of gestation (relative
to normal length) were inversely associated with RMS risk.
The association of higher birth weight and RMS risk among only
non-Hispanic whites may reflect differences by race and ethnicity.
It may also reflect the inability of birth weight to capture fetal
growth rates during etiologically relevant time periods. It is known
that birth weight [12e14] differs by race and ethnicity, with black,
Asian, and Hispanic infants having lower gestational age-adjusted
birth weight than non-Hispanic whites. However, an analysis of
U.S. birth records of Mexican American and non-Hispanic whites
from 1994 to 1996 found that Mexican American infants were
heavier than non-Hispanic white infants between 30 and 37 weeks
of gestation, whereas non-Hispanic whites were heavier at or after
42 weeks gestation [15], suggesting that intrauterine growth pat-
terns [13] differ by ethnic group. It remains unknown how various
lifestyle, environmental, and genetic factors contribute to this
variation.
Because RMS is a sarcoma thought to originate from muscle cell
progenitor cells, with differentiation into primary and secondary
muscle fibers occurring during the embryonal and early and mid-
fetal stage [16], fetal growth during these stages may be more
relevant than birth weight, which may reflect late (>37 weeks)
gestation weight gain after muscles are fully developed. Therefore,
although the utility of high birth weight as an independent risk
factor for RMS is unclear, a role of fetal growth patterns in the
etiology of pediatric RMS remains plausible. Insulin-like growth
factors (IGFs) play a major role in fetal growth and development,
with IGF1 being the principal IGF in late fetal development and
adult growth and IGF2 being the primary IGF active in early fetal
development. Genes in the IGF axis, as well as in intersecting
growth related pathways, are highly polymorphic, and genetic
variation may play an important role in pediatric RMS
development.
The information collected on birth certificates, which varies
between states and by year, does not contain the data elements
necessary to accurately assess fetal growth patterns, such as
maternal weight gain, fundal height, and sonograms throughout
pregnancy. It has been suggested that proportion of optimal birth
weight (POBW) may be a more suitable measure of appropriateness
of fetal growth from neonatal birth records [17]. Perhaps due to
limitations of data available from California birth certificates, the
models developed to predict POBW using the method described in
Blair et al. [17] explained only approximately 27% of the variation in
outcome measure (adjusted R-squared ¼ 0.2723), and we did not
include POBW as an independent predictor in our analyses.
This study presents several strengths, including the large sample
size, ethnic diversity, and unbiased data collection from cases and
controls. There are some limitations, however, that should be
considered. First, given the design of the study, our conceptualized
birth cohort did not include cases who were diagnosed in California
but born elsewhere, but it is possible that some of the controls
could have moved from California, been diagnosed with RMS
outside California, and, therefore, not linked to the CCR. Given the
rarity of RMS, the chance of this is low. In addition, there are no data
to suggest that such out-migration is associated with our exposures
of interest (birth weight, gestational age). Second, the accuracy of
birth certificate data is known to vary widely, with measures
of maternal risk factors and comorbidities and complications of
pregnancy, labor and delivery having the lowest agreement in a
comparison of birth certificates with medical records [18]. The in-
dependent predictor and adjustment covariates focused on in our
report, however, were birth characteristics (birth weight, gesta-
tional age) that have excellent (>90%) agreement [19]. Finally,
changes in the histologic definition of aRMS over the years [20], the
lack of central adjudication of cancer registry cases and differences
in diagnosing institution practices may have led to misclassification
 L.M. Morimoto et al. / Annals of Epidemiology xxx (2015) 1e5
of our subtype-stratified results and reduced the precision of our
estimates. Although a limitation, the large sample sizes of rare
cancers and the robust estimates permitted by using registry link-
ages still make meaningful contributions to the literature.
In this study, we observed an indication of association between
high birth weight, LGA, and an increased risk of total RMS and eRMS
among non-Hispanic white children and adolescents, but not other
racial or ethnic groups. Studies in racially diverse populations are
essential for uncovering differing environmental factors that
impact disease risk. Analyses incorporating genetic markers and
genetic ancestry are underway in this study population to further
evaluate the etiology of this still poorly understood pediatric
malignancy.
Acknowledgments
The Alex’s Lemonade Stand Foundation (ALSF; award 034816)
funded the study.
Additional support was provided to Dr. Morimoto by the Na-
tional Institute of Environmental Health Sciences (NIEHS), USA (P01
ES018172) and the Environmental Protection Agency, USA (USEPA,
RD83451101), as part of the Center for Integrative Research on
Childhood Leukemia and the Environment (CIRCLE). The content is
solely the responsibility of the authors and does not necessarily
represent the official views of the ALSF, NIEHS, or USEPA.
The collection of cancer incidence data used in this study was
supported by the California Department of Public Health as part of
the statewide cancer reporting program mandated by California
Health and Safety Code Section 103885; the National Cancer In-
stitute’s Surveillance, Epidemiology and End Results Program under
contract HHSN261201000140C awarded to the Cancer Prevention
Institute of California, contract HHSN261201000035C awarded to
the University of Southern California, and contract
HHSN261201000034C awarded to the Public Health Institute; and
the Centers for Disease Control and Prevention’s National Program
of Cancer Registries, under agreement U58DP003862-01 awarded
to the California Department of Public Health. The ideas and
opinions expressed herein are those of the author(s) and
endorsement by the State of California, Department of Public Health
the National Cancer Institute, and the Centers for Disease Control
and Prevention or their Contractors and Subcontractors is not
intended nor should be inferred.
5
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